Sarkadi B, Mack E, Rothstein A
J Gen Physiol. 1984 Apr;83(4):513-27. doi: 10.1085/jgp.83.4.513.
Hypotonic dilution of human peripheral blood lymphocytes (PBL) induces large conductive permeabilities for K+ and Cl-, associated with the capacity of the cells to regulate their volumes. When rapid cation leakage is assured by the addition of the ionophore gramicidin, the behavior of the anion conductance pathway can be independently examined. Using this technique it is demonstrated that the volume-induced activation of Cl- transport is triggered at a threshold of approximately 1.15 X isotonic cell volume. If the volume of a cell is increased to this level or above, the Cl- transport system is activated, whereas if the volume of a swollen cell is decreased below the threshold value, the Cl- transport is inactivated. Activation and inactivation are independent of the relative volume changes and of the actual cellular Na+, K+, or Cl- concentrations, as well as of the changes in membrane potential in PBL. When net salt movement and thus volume change are inhibited by specific blockers of K+ transport (e.g., quinine, or Ca2+ depletion), volume-induced Cl- conductance shows a time-dependent inactivation, with a half-time of 5-8 min. The Cl- conductance, when activated, appears to involve an all-or-none response. In contrast, volume-induced K+ conductance is a graded response, with the increase in K+ flux being roughly proportional to the hypotonicity-induced increase in cell volume. The data indicate that during lymphocyte volume response in hypotonic media, anion conductance increases by orders of magnitude, exceeding the K+ conductance, so that the rate of the volume decrease (KCl efflux) is determined by a graded alteration in K+ conductance. When the cell volume approaches the isotonic value, it is stabilized by the inactivation of the anion conductance pathway.
人外周血淋巴细胞（PBL）的低渗稀释会诱导K⁺和Cl⁻产生大的传导通透性，这与细胞调节其体积的能力相关。当通过添加离子载体短杆菌肽确保快速阳离子泄漏时，阴离子传导途径的行为可以独立研究。使用该技术表明，Cl⁻转运的体积诱导激活在约1.15倍等渗细胞体积的阈值处触发。如果细胞体积增加到该水平或更高，则Cl⁻转运系统被激活，而如果肿胀细胞的体积减小到阈值以下，则Cl⁻转运被灭活。激活和失活与相对体积变化、细胞内实际的Na⁺、K⁺或Cl⁻浓度以及PBL中膜电位的变化无关。当K⁺转运的特异性阻滞剂（如奎宁或Ca²⁺耗竭）抑制净盐运动从而抑制体积变化时，体积诱导的Cl⁻电导显示出时间依赖性失活，半衰期为5 - 8分钟。Cl⁻电导激活时似乎涉及全或无反应。相反，体积诱导的K⁺电导是一种分级反应，K⁺通量的增加大致与低渗诱导的细胞体积增加成比例。数据表明，在低渗介质中淋巴细胞体积反应期间，阴离子电导增加几个数量级，超过K⁺电导，因此体积减小速率（KCl外流）由K⁺电导的分级改变决定。当细胞体积接近等渗值时，它通过阴离子传导途径的失活而稳定。
